Lithium & antidepressants better than ARVs for XMRV, & more

Yesterday I was talking with an expert doctor on VIH/AIDS and on ME/CFS, who explained how antidepressants worked better than ARVs for VIH. (See abstract below).

Also told me that autophagy inhibition was the clue for antiretrovirology theraphy, and that this phenomenon could perfectly well be assessed by other therapies than ARV's, MUCH safer...(I wrote back him asking how...).

He is interested in GcMAF, and I will be updating him about my evolution on this treatment.

The ability to safely and economically stimulate immune function would transform the humanitarian and
economic landscapes of nosocomial, surgical and antibiotic-resistant infections, as well as reduce the burden of
epidemics, pandemics and bioterrorism. Such stimulation is widely held to be beyond our reach, an unfortunate
misconception. As early as the mid 1980s sufficient evidence had accumulated to be able to state with conviction that
lithium and antidepressants have these properties. Excessive production of prostaglandin E2 activates microorganisms
and suppresses immune function, and lithium and antidepressants oppose prostaglandin E2. Immunostimulation is nonspecific,
possibly relevant to all infections, pertinent to one, two, or more concurrent infections, and highly cost/
effective. In controlled studies an antidepressant would be relevant to that agent and only that agent, rendering such
studies worthless. Over the past twenty years 22 drug companies have declined interest in developing antidepressants
as antiinfectives. It would be unethical to deny the infected these well documented benefits.
c 2006 Elsevier Ltd. All rights reserved.

It seems like we have to be careful with antidepressants though. For instance, this paper below talks about how antidepressants can increase the proinflammatory cytokine IL-6, which likely would be bad for us.

Yi-Chyan Chen,1 Wei-Win Lin,1 Yu-Jung Chen,2 Wei-Chung Mao,1 and Yi-Jen Hung3.* Antidepressant Effects on Insulin Sensitivity and Proinflammatory Cytokines in the Depressed Males. Mediators Inflamm. 2010; 2010: 573594.
Growing evidence suggests that mood disorder is associated with insulin resistance and inflammation. Thus the effects of antidepressants on insulin sensitivity and proinflammatory responses will be a crucial issue for depression treatment. In this study, we enrolled 43 non-diabetic young depressed males and adapted standard testing procedures to assess glucose metabolism during 4-week hospitalization. Before and after the 4-week antidepressant treatment, participants underwent oral glucose tolerance test (OGTT) and frequently sampled intravenous glucose tolerance test (FSIGT). Insulin sensitivity (SI), glucose effectiveness (SG), acute insulin response, and disposition index (DI) were estimated using the minimal model method. The plasma levels of C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and adiponectin were measured. The Hamilton depression rating scale (HAM-D) total scores were reduced significantly during the course of treatment. There were no significant changes in the parameters of SI, SG, and DI. Compared to drug nave status, the level of plasma IL-6 was significantly elevated (0.77 to 1.30pg/ml; P = .001) after antidepressant therapy. However, the concentrations of CRP, TNF-α, and adiponectin showed no differences during the course of treatment. The results suggest that antidepressants may promote stimulatory effect on the IL-6 production in the early stage of antidepressant treatment.http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2872762/

Immune modulators seem tricky. There are a whole bunch of different components, and if you don't look at all of them the potential is there to choose ones that make things worse.

I've not heard of many ME/CFS patients being helped by antidepressants. Obviously reports of what has helped people are subjective, but insofar as ME/CFS patients report positively on a particular substance, I'm inclined to take that into consideration.

In the short term, both Lamictal (an anticonvulsant that serves to elevate and stabilize the mood) and small amounts of lithium have been good for me. Whether they have been good or bad in the long-run, it's hard to know.

Here's a paper that talks about E2.

Rapoport SI, Basselin M, Kim HW, Rao JS. Bipolar disorder and mechanisms of action of mood stabilizers. Brain Res Rev. 2009 Oct;61(2):185-209. Epub 2009 Jun 23.
Bipolar disorder (BD) is a major medical and social burden, whose cause, pathophysiology and treatment are not agreed on. It is characterized by recurrent periods of mania and depression (Bipolar I) or of hypomania and depression (Bipolar II). Its inheritance is polygenic, with evidence of a neurotransmission imbalance and disease progression. Patients often take multiple agents concurrently, with incomplete therapeutic success, particularly with regard to depression. Suicide is common. Of the hypotheses regarding the action of mood stabilizers in BD, the "arachidonic acid (AA) cascade" hypothesis is presented in detail in this review. It is based on evidence that chronic administration of lithium, carbamazepine, sodium valproate, or lamotrigine to rats downregulated AA turnover in brain phospholipids, formation of prostaglandin E(2), and/or expression of AA cascade enzymes, including cytosolic phospholipase A(2), cyclooxygenase-2 and/or acyl-CoA synthetase. The changes were selective for AA, since brain docosahexaenoic or palmitic acid metabolism, when measured, was unaffected, and topiramate, ineffective in BD, did not modify the rat brain AA cascade. Downregulation of the cascade by the mood stabilizers corresponded to inhibition of AA neurotransmission via dopaminergic D(2)-like and glutamatergic NMDA receptors. Unlike the mood stabilizers, antidepressants that increase switching of bipolar depression to mania upregulated the rat brain AA cascade. These observations suggest that the brain AA cascade is a common target of mood stabilizers, and that bipolar symptoms, particularly mania, are associated with an upregulated cascade and excess AA signaling via D(2)-like and NMDA receptors. This review presents ways to test these suggestions.
PMID: 19555719 [PubMed - indexed for MEDLINE]

It seems to me that this article is suggesting that antidepressants that increase bipolar switching into mania (which includes basically all antidepressants except for the MAO-I's and maybe Wellbutrin) actually could upregulate prostaglandin E2. I will read the paper more closely later to see if that's indeed what they're saying.

ME/CFS actually has a lot in common with bipolar. Both diseases seem to be massively affected by inflammatory substances such as biotoxins, for instance. Looking more at substances that help in bipolar thus might be useful in considering what might be useful in this disease as well, possibly.

This is a really good line of thought. I'm going to do some more reading, as well as think about increasing the amount of lithium I've been taking. Just 5 mg of lithium orotate has been such a good thing for me that maybe a larger amount is warranted. I'd been thinking that already, and this makes me more inclined to try.

Yes, and they also deplete serotonine on the medium term, affect the mitochondria, etc. What the doctor was telling me is that, after many years of practice, he is finding antidepressants a much better approach for AIDS patiences that ARVs...It's just an opinion, but I do know he treats lots of HIV/AIDS patients...

I am not defending the use of antidepressants for CFS, with, or without XMRV. But thought this was very interesting.

Also, I think what is even more interesting is the idea about the autophagy inhibition, as one of the clues for the antoretroviral treatment, and the fact that this can be accomplished with safer treatments. He was telling me how many AIDS patients die with high CD4+, although I couldn't understand the relationship between this and autophagy inhibition...I read that this process is induced by VIH in uninfected cells, but still have not had time to figure this out:

I am taking the anti-depressant Amitriptyline and it's one of the drugs that has improved my condition. Amitriptyline is anti-inflammatory, so yeah that might be helping (I have noticed that every drug or supplement that is anti-inflammatory has helped my condition). Unfortunately, antidepressants don't seem to work for everyone. I know the first time I took Amitriptyline I felt like I was shot with a stun gun...

Yes, and they also deplete serotonine on the medium term, affect the mitochondria, etc. What the doctor was telling me is that, after many years of practice, he is finding antidepressants a much better approach for AIDS patiences that ARVs...It's just an opinion, but I do know he treats lots of HIV/AIDS patients...

I am not defending the use of antidepressants for CFS, with, or without XMRV. But thought this was very interesting.

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The difference is that, to my knowledge, HIV/AIDS patients don't have the runaway cytokine problem that we do. (Has anyone heard a theory on why XMRV might give us that particular problem? Does it destroy anti-inflammatory cytokines in some way, maybe?)

I think that the idea of doing things like controlling PGE2 is a really good one. It just sounds like (as is always the case with ME/CFS) there may be some drugs that are much more appropriate than others for us, in terms of trying to accomplish a particular goal.

Are indeed antidepressants like Amitriptyline (Elavil) anti-inflammatory? All the anti-depressants I've ever taken felt extremely pro-inflammatory to me, but maybe other people have different experiences.

I've done really badly on antidepressants. Made me much worse and for a very long time, every time. Tried amittrip, prozac and others. This is something I would avoid unless I had no other choice (and only try ones that I hadn't before). Fortunerly I am not depressed and only tried them previously due to be "sold" them as sleep aids, painkillers etc. They didn't even work for that.

The difference is that, to my knowledge, HIV/AIDS patients don't have the runaway cytokine problem that we do. (Has anyone heard a theory on why XMRV might give us that particular problem? Does it destroy anti-inflammatory cytokines in some way, maybe?)

I think that the idea of doing things like controlling PGE2 is a really good one. It just sounds like (as is always the case with ME/CFS) there may be some drugs that are much more appropriate than others for us, in terms of trying to accomplish a particular goal.

Are indeed antidepressants like Amitriptyline (Elavil) anti-inflammatory? All the anti-depressants I've ever taken felt extremely pro-inflammatory to me, but maybe other people have different experiences.

Best, Lisa

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Hi Lisa i don't think XMRV destroys citokines it's actually the opposite cytokines fight infections and that's why inflammation occurs, for instance when the virus reaches the brain the cytokines go to your brain to fight the virus which results in a never ending battle which of course turns into autoimmune because you can't flush the virus out of the brain so the cytokines are always there fighting the virus and that's why brain demyelination and brain lesions happen, HIV+ people do have an inflammation problem because of the cytokines what helps them a lot is that they have effective treatments to lower the viral load most of the times to an undetected viral load by PCR, so the cytokines don't do their job because they don't need to, a good evidence as how the cytokines work and hopefully this will explain better is how HIV+ people don't get brain demyelination because of HIV(due to undetected viral load) but because infection with JC virus which of course activates cytokines to go to the brain to fight the JC virus and that's when HIV+ people get brain demyelination, lesions and sometimes PML, so to make it short the meds are doing their job to control HIV but not very well to control JC virus which activates the cytokines, so i think as they come up with some good meds that stop XMRV replication the inflammation problem will be solved, another possible theory is that XMRV does not transform cells as fast as HIV so im thinking maybe since the virus does not replicate as fast the cytokines are trying really hard to fight the infection which results in inflammation with HIV the replication is so fast most of the time tat maybe the cytokines don't stand a chance to fight it...

When people say "cytokines," they usually mean "pro-inflammatory cytokines."

But there also are "anti-inflammatory cytokines." They're not discussed nearly as much, but (per Shoemaker) I wonder if problems with them might be in part responsible for why the inflammation is such a problem in this disease.

Just a thought, and not one that's particularly related to this thread. Sorry to have provided the distraction.

Are indeed antidepressants like Amitriptyline (Elavil) anti-inflammatory? All the anti-depressants I've ever taken felt extremely pro-inflammatory to me, but maybe other people have different experiences.

Best, Lisa

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Yes, Amitriptyline is anti-inflammatory. It's a side effect though, not its main use.

Excessive production of prostaglandin E2 activates microorganisms and suppresses immune function, and lithium and antidepressants oppose prostaglandin E2. Immunostimulation is nonspecific, possibly relevant to all infections, pertinent to one, two, or more concurrent infections, and highly cost/effective. It would be unethical to deny the infected these well documented benefits.

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Hi, I have been involved in, or used, E2 controlling strategies for CFS since 1993. Antidepressants are not the only way to go. E2 is made from the omega-6 fat arachidonic acid, which is excessively utilized in CFS. I have posted at length, repeatedly, on this topic. Omega-3s, extra-virgin olive oil, and avoiding meat fats (but not lean meats) and organ meats are the way to go here - all involve a simple change in diet, with minimal side effects.

The success rate at the only clinic I know of to try this was 60% high (return to work), 30% partial, 10% fail. The doctor was prosecuted because "there is no treatment for CFS" and forced out of treating CFS patients. Autonomic and metabolic testing was regularly done on all patients, and was used as a guide for adjusting the diet. This started in the late 80s, and was shut down by 1995. Success went with improved autonomic function and higher metabolic rates.

I am going to run the test of inflammatory cytokines, as seems to be a basic test Dr. De Meirleir prescribes (I'll post my results as soon as I receive them). According to some of his interviews, as XMRV load is reduced, inflammatory cytokines lower, as does C4a (key marker of the complement system).

Of course there's inflammation on HIV infection, as there is in any other infection...Anti-inflammatory cytokines serve for controlling the inflammatory response. I have never heard of a problem caused for an excess of the latest....have you?

I am just hoping we can get off of Amitriptyline when the time comes. An ex girlfriend has CFS as well and has been on antidepressants for 4 years. She can't stop taking them, because she gets all kind of mental issues. She feels delusional for example. She didn't have mental issues before taking the anti-depressant...

Hi I have a thread on cycloferon which is an interferon inducer, it mainly stimulates alpha and beta interferon which have anti-inflammatory effects where gamma interferon has pro inflammatory effects, i think this is why cycloferon has helped me alot. Some of the bad side effects of interferon treatments are due to gamma interferon and it causes viral like symptoms although all interferons have antiviral properties. Immunovir is another interferon inducer that has these same anti-inflammatory effects. Interferon i think can be classed as a cytokine or maybe a cytokine stimulant.

When people say "cytokines," they usually mean "pro-inflammatory cytokines."

But there also are "anti-inflammatory cytokines." They're not discussed nearly as much, but (per Shoemaker) I wonder if problems with them might be in part responsible for why the inflammation is such a problem in this disease.

Just a thought, and not one that's particularly related to this thread. Sorry to have provided the distraction.

Hi, I have been involved in, or used, E2 controlling strategies for CFS since 1993. Antidepressants are not the only way to go. E2 is made from the omega-6 fat arachidonic acid, which is excessively utilized in CFS. I have posted at length, repeatedly, on this topic. Omega-3s, extra-virgin olive oil, and avoiding meat fats (but not lean meats) and organ meats are the way to go here - all involve a simple change in diet, with minimal side effects.

The success rate at the only clinic I know of to try this was 60% high (return to work), 30% partial, 10% fail. The doctor was prosecuted because "there is no treatment for CFS" and forced out of treating CFS patients. Autonomic and metabolic testing was regularly done on all patients, and was used as a guide for adjusting the diet. This started in the late 80s, and was shut down by 1995. Success went with improved autonomic function and higher metabolic rates.

Bye
Alex

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Wow, another person who's heard that "If you found something that worked, you must never have been sick" logic. Apparently people used to say that to Erik all the time about the mold avoidance.

Omega-3 oils have been shown to have positive effects on bipolar too. I never understood this until now.

Another thing that people use to help bipolar is lecithin (phos choline). I wonder if the mechanism for that is the same.

My understanding is that the problem with meat is only if it's grain fed. Grass fed animals produce meat (and eggs/milk) that is relatively high in Omega-3's, I think.

This is an excellent idea. My hands are feeling very dry at the moment, so I'm going to start chugging the fish oil to see if I can get things back in sync. Who knows, maybe it will have a positive benefit on the viruses too.

I am going to run the test of inflammatory cytokines, as seems to be a basic test Dr. De Meirleir prescribes (I'll post my results as soon as I receive them). According to some of his interviews, as XMRV load is reduced, inflammatory cytokines lower, as does C4a (key marker of the complement system).

Of course there's inflammation on HIV infection, as there is in any other infection...Anti-inflammatory cytokines serve for controlling the inflammatory response. I have never heard of a problem caused for an excess of the latest....have you?

Regards,
Sergio

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Erik corresponds frequently with Ritchie Shoemaker, and he thus seems to have a grasp of Shoemaker's theories that can be difficult to glean elsewhere. I'm putting a comment of his below.

The concept of anti-inflammatory cytokines seems right to me, in terms of my experience. It's not so much that I have too many proinflammatory cytokines when I get hit with mold, though maybe that's true too. It's more that whatever reaction I get when I am hit with mold is like a runaway train. It keeps barreling on until I take great pains to get wholly clear, even if I continue to be exposed to just tiny amounts.

I don't think that's what's supposed to happen. I think that the inflammation is to be expected. It's just not supposed to go on forever. There's supposed to be a brake.

So if the question is why the anti-inflammatory "brake" isn't working, then I have to wonder if XMRV could be part of the mix. Could it be that the virus makes them go away? How might that work?

Is there any evidence that ME/CFS patients have an insufficiency of anti-inflammatory cytokines?

Thanks, Lisa

*

Dr. Shoemaker describes how the prolonged inflammatory response continually removes more anti-inflammatory cytokines. Theoretically, if one had all their anti-inflammatory responses neutralized, there would be nothing from stopping one single spore from creating an all-out systemic over-response. But the good news is that the longer one can stay damped down, it appears that the anti-inflammatory responses might be restored.

At least that's how it's been for me. By extreme avoidance for a portion of the time, I build up a certain degree of tolerance for other times when I have to enter mold zones. This wild variability of
pro- and anti-inflammatory cytokines seems to be how people can go through various degrees of reactivity that are so insanely out-of-whack with the "dose-response" model of illness.

Not sure if the following anecdotal story is relevant (haven't read this whole thread), but thought I'd post it anyway, just because I think it's interesting.

I have a friend who has major mold sensitivities, major MCS/EI, and feels he has a significant blood brain barrier (BBB) component to his fragile health. Though he's homeless and lives out of his van, he seems to have find a number of coping strategies that have helped him a lot. He used to consider he had ME/CFS, because he had so many symptoms, but as I've gotten to know him, I realize he's far more functional than I am.

Anyway, he told me his experience from a few years ago, when he was still seeing doctors to help him with his myriad health problems. One doctor finally prescribed lithium for him. I'm not sure if it was for depression per se, or for some of his other health issues.

Well, as soon as he tried the lithium prescription (50 mg. if I remember correctly), he had a terrible reaction to it. I don't recall if he ever took it again, but if so, it was for a very short time because of how intensely uncomfortable it was.

A short while later, he saw lithium at a nutritional supplement dept. at the local CO-COP, and noticed the dosage was about 1% or so of the prescription lithium he had gotten. So he decided to give it a try. Turns it, it was a miraculous turning point for him. I don't recall all the details, but I wonder if it might have been just the right amount to stimulate his immune system to bring about better overall health and functionality.

I'm going to try to remember to ask him about this again, as it's been years since we first discussed it. Who knows, could be relevant for some of us.

Hi, I have been involved in, or used, E2 controlling strategies for CFS since 1993. Antidepressants are not the only way to go. E2 is made from the omega-6 fat arachidonic acid, which is excessively utilized in CFS. I have posted at length, repeatedly, on this topic. Omega-3s, extra-virgin olive oil, and avoiding meat fats (but not lean meats) and organ meats are the way to go here - all involve a simple change in diet, with minimal side effects.

The success rate at the only clinic I know of to try this was 60% high (return to work), 30% partial, 10% fail. The doctor was prosecuted because "there is no treatment for CFS" and forced out of treating CFS patients. Autonomic and metabolic testing was regularly done on all patients, and was used as a guide for adjusting the diet. This started in the late 80s, and was shut down by 1995. Success went with improved autonomic function and higher metabolic rates.

Bye
Alex

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Often lost in this discussion however is the fact Omega 6 fats are not all bad, in fact GLA from evening primrose oil (preferred) or borage oil are absolutely essential in order to make E1 (anti-inflammatory) prostaglandins. One can take all the fish, flax and other EFA's by the gallon (to get their EPA's), but they won't do any good if GLA isn't present in the first place.

Yes, most people these days consume way too much Omega 6 fats from eating too many processed foods, junk foods, salad dressings, etc.. But that doesn't mean everyone does.

Patricia Kane PhD has worked with thousands of chronically ill patients -- mostly autistic children, but also MS, CFS, ALS, etc -- and has found, through fatty acid panels run at Johns Hopkins -- that almost 90% of them had too much omega 3's, and surprisingly not enough omega 6 fats. She contends that if one has high O-3's and low O-6's, then one must replete O-6 with evening primrose oil for several weeks before adding omega 3's. It's interesting that one of the measures they use to judge how treatment is coming along is the Visual Contrast Sensitivity Test (the same as Shoemaker?). Here's just one link to her work:

Balance is the key, but you must have both in order to make the so-called "good" prostaglandins.

I had a fatty acid analysis done as part of a NutrEval panel. It showed that my Omega-3's were indeed too high and my omega 6 levels were too low.

I kind of didn't take it seriously enough and/or forgot about it until just a few days ago but have now started some evening primrose oil. Hopefully my classic O-6 deficiency symptoms (extremely dry skin, dry eyes, eczema, dehydration, severe mood swings, ADD, anxiety, hyperactivity, joint problems, neuropathy, impaired wound healing -- all increasingly worse over the past 3+ months when I ran out of the EPO) will begin to resolve in a few weeks. I was seriously ready to jump out the window.

Just my two cents,

Dan

p.s. I think Lisa posted on another page that MCS patients had lower levels of omega 6 than controls.

Hi Wayne, it would be good to hear whether low dose lithium could help. Sometimes docs don't get to hear about off label uses of drugs, especially after the patent with the original drug company making the drug expires (and anyone can then make it), because there is no advantage/profit for them/anyone.

I remember an article someone wrote back in the 50s/60/s about off label use of an Epilepsy drug (Dilantin) - for mood disorders. It was trialled in prisons for eg (double blind, placebo etc) and was incredibly successful as a mood balancer in helping distressed and violent inmates regain their emotional equilibrium (they reported being happy!), but no one was interested, including the manufacturers, presumably because more money was to be made for everyone from the newer antidepressants/valium etc - which seemed to be less effective.

Often lost in this discussion however is the fact Omega 6 fats are not all bad, in fact GLA from evening primrose oil (preferred) or borage oil are absolutely essential in order to make E1 (anti-inflammatory) prostaglandins. One can take all the fish, flax and other EFA's by the gallon (to get their EPA's), but they won't do any good if GLA isn't present in the first place.

Yes, most people these days consume way too much Omega 6 fats from eating too many processed foods, junk foods, salad dressings, etc.. But that doesn't mean everyone does.

Patricia Kane PhD has worked with thousands of chronically ill patients -- mostly autistic children, but also MS, CFS, ALS, etc -- and has found, through fatty acid panels run at Johns Hopkins -- that almost 90% of them had too much omega 3's, and surprisingly not enough omega 6 fats. She contends that if one has high O-3's and low O-6's, then one must replete O-6 with evening primrose oil for several weeks before adding omega 3's. It's interesting that one of the measures they use to judge how treatment is coming along is the Visual Contrast Sensitivity Test (the same as Shoemaker?). Here's just one link to her work:

Balance is the key, but you must have both in order to make the so-called "good" prostaglandins.

I had a fatty acid analysis done as part of a NutrEval panel. It showed that my Omega-3's were indeed too high and my omega 6 levels were too low.

I kind of didn't take it seriously enough and/or forgot about it until just a few days ago but have now started some evening primrose oil. Hopefully my classic O-6 deficiency symptoms (extremely dry skin, dry eyes, eczema, dehydration, severe mood swings, ADD, anxiety, hyperactivity, joint problems, neuropathy, impaired wound healing -- all increasingly worse over the past 3+ months when I ran out of the EPO) will begin to resolve in a few weeks. I was seriously ready to jump out the window.

Just my two cents,

Dan

p.s. I think Lisa posted on another page that MCS patients had lower levels of omega 6 than controls.

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Three years ago, just before moving out of my moldy house, I had an Individualized Optimal Nutrition from MetaMetrix. They tested something like 20 different fatty acid measures and recommended to me something like 6 capsules of black currant seed oil (which is GLA) per day. They said nothing about EPA's.

I've periodically taken that, but not as much and not regularly. And I've not looked into this much.

I've recently started thinking about this because I've been focusing less on the inflammatory component of my disease (which seems to be starting to come under control, apparently due to detox and/or pathogen control as well as extended avoidance) and more on the glutamate component (which still is almost as high as it's ever been). The glutamate component is associated with symptoms like "Sensory Storms" (prefrontal lobe cortical seizures) and heart issues and (at least in my case) a particular biotoxin found outdoors.

(The article you pointed out talks about both biotoxins and heavy metals as being factors here, Dan.)

Upon reflection, the glutamate activity seems to me not unrelated to the phenomenon of rapid-cycling bipolar, a diagnosis (misdiagnosis?) I had early in my illness. This is a poorly understood condition that (like ME/CFS and mold illness) is rapidly increasing in the population, especially in women.

In the spirit of this "let's fix our own illness" mentality, in 1998 I found a tiny scale experiment where some people seemed to be benefiting from using Lamictal. My psychopharmacologist wouldn't try it, so I got Dale Guyer (my ME/CFS physician) to let me try it. It stabilized my moods really well with no side effects. (Now the same psychopharmacologist uses it as his first-line treatment on all patients. Think of all the years I'd have wasted waiting for him!)

The Lamictal took away the severe symptoms (suicidal depressions, screaming rages and feelings like my brain was going to shatter into a million little pieces), which was a good thing. But this component of my system still feels off-balance, especially when I am being hit with this glutamate-affecting outdoor biotoxin (which, since I'm not sure what it is, I've been calling the "?") but even on a constant basis when experiencing feeling of excitotoxicity (a key component of Amy Yasko's approach to autism).

As time went on and I became mostly catatonic (and then, after avoidance, hyperreactive) from increased inflammation, this issue became buried. Now it's come more front and center again.

(My fear when I bring up the bipolar stuff is that people are going to dismiss the idea that I actually have ME/CFS, even though I have a truckload of tests showing 100% consistency with classic ME/CFS. I now think that they're components of the same thing and that most ME/CFS patients are more "bipolar" than they think, that it's triggered by this biotoxin, and that the periodic meltdown of all these ME/CFS boards is a component of that.)

The interesting thing is that all the treatments for rapid-cycling bipolar (the kind that doesn't involve psychosis) are the things we're mentioning here: anticonvulsants such as Lamictal (lamotrigine), lithium, large amounts of omega-3 and (in the article Dan brought up) large amounts of phosphatidyl choline.

When I look at that list, it makes me think that if supplements work well enough to get into the published literature, it must be because something related to those supplements is messed up. That article Dan recommended (which actually is really good) is the first time I've seen a comprehensive explanation why.

I recently started taking some phos choline (which is supposed to heal the outer component of the cell membrane) and am thinking that the lack of it has been a huge missing component for me.

Reading this article, I can see why Omega 6's might be deficient. Most oils that people consume (such as canola or peanut) actually create renegade fatty acids that disrupt the membranes, and thus are very bad. (Note that viruses and other pathogens contribute to the proliferation of more renegade fats.)

Olive oil, which (I think) is Omega 9, is neutral. Butter and animal fat is a mix of Omega 6 (I think the good kind?) and Omega 3 (far more Omega 3 if grass-fed).

(Unfortunately, restaurant food is primarily the bad renegade fats. This is a reason not to eat out, which I have been doing way too much.)

Early in the summer, I took a lot of black currant seed oil. This did weird things to my skin, making me think that I didn't need it. I focused more on flax/fish oil. But recently I've been experiencing cravings for butterfat, which makes me think I've moved to needing more omega 6.

This is a little confusing. How do I know what I need, other than getting that lab test done repeatedly?

What is the difference between GLA (present in black currant seed, borage seed and evening primrose oils) and Omega 6?

If I just take a lot of both Omega 3 and GLA, continue to consume Omega 6 (e.g. in butterfat and in the "Udo's Choice" oil I just bought), and try to eliminate the renegade fats, would that be sufficient?

I would think that the body would have a regulating mechanism to use the fats available as needed, so that the proportions I consume aren't so crucial. But maybe that's not the case, or mine is broken.

This seems like a really important component of our illness. I wish we could figure out how the viruses and other pathogens tie into it.

That's a really good article you found, Dan. Maybe we should have a further discussion about it elsewhere on this board.